A new report links remnants of a once-common pesticide to lung infections and wheezing in kids exposed to the chemical before birth.

Known as DDE, the compound is a broken-down form of the harmful pesticide DDT and is found in many places around the world. it is absorbed into a person’s body when they eat contaminated food or breathe contaminated dust.

The study, published in the European Respiratory Journal, shows babies exposed to high levels of DDE in the womb grew up to have higher rates of pneumonia and bronchitis.

“We found that the risk of infections and wheeze increased with increasing DDE exposure,” Martine Vrijheid, associate professor at the Centre for Research in Environmental Epidemiology in Spain, told Reuters Health by email.

Vrijheid and her colleagues took blood samples from a large group of pregnant women in Spain, measuring the women’s exposure to three different pollutants.

Later, when the babies were about a year old, the researchers asked the mothers whether their toddlers had had breathing trouble or lung infections.

About 35 percent of the 1,342 children developed a lung infection within their first year, the team found, and the risk rose in tandem with the DDE levels in the mother’s blood.

Vrijheid estimates that with undetectable or very low levels of DDE, only 30 percent of the children would have developed infections.

The new study is the largest of its kind, according to the researcher. Past work has yielded mixed results, and until now has failed to show a significant association between DDE exposure and lung infections within a child’s first year of life.

DDT was once widely used to kill mosquitoes and prevent malaria outbreaks, but its use was called into question in the 1960s and was banned in the U.S. in 1973. But it and its breakdown products can last in the environment for hundreds of years.

People exposed to large amounts of DDT may experience tremors, seizures, sweating, headaches and vomiting, according to the Centers for Disease Control and Prevention. But those symptoms disappear when the person is no longer exposed to the pesticide.

Barbara Cohn, the director of Child Health and Development Studies at the Public Health Institute in California, told Reuters Health that DDT and its remains have been hard to study because of the time needed for it to show up in people.

“People thought it was a miracle compound,” said Cohn. “Nobody really knew what might be happening.”

DDT is still used in some parts of the world, because it is considered the best way to kill malaria-carrying mosquitoes, said Vrijheid.

In 2006, the World Health Organization sanctioned an altered technique for using DDT, which involves spraying the pesticide on the inside of a building to kill mosquitoes that land on its walls and other surfaces.

Vrijheid told Reuters Health that it’s hard to avoid chemicals like DDT and DDE, which are stored in fat and found in higher concentrations at the top of the food chain.

“One way of reducing exposure is by reducing the consumption of fatty foods and increasing the consumption of vegetables and fruits,” she said. “This does not mean we should stop eating meat, yogurts or certain types of fish, but just that we should have (a balanced) diet.”

ROME — In a clinical trial that dramatically confirmed years of observation, early use of antiretroviral therapy reduced the risk of transmitting HIV between couples. the approach also reduces the risk of clinical symptoms of HIV infection, although not to the same degree, according to Myron Cohen, MD, of the University of North Carolina Chapel Hill, and colleagues. the findings support the use of antiretroviral therapy as a public health measure to slow the rate of HIV transmission, Cohen and colleagues reported online in the new England Journal of Medicine and at the International AIDS Society conference here.Action Points  

• Explain that in a clinical trial that dramatically confirmed years of observation, early use of antiretroviral therapy reduced the risk of transmitting HIV between couples.
• Note that the approach also reduces the risk of clinical symptoms of HIV infection.

“The study demonstrates a terrific benefit from earlier therapy,” Cohen told MedPage Today. “It’s quite simple – there’s a clinical benefit for the patient and a dramatic, nearly 100%, reduction in transmission.”

The key question now, he added, is how to best use the knowledge to slow the progress of the HIV/AIDS pandemic.

That’s especially true because “we don’t have enough resources” to treat all those for whom therapy is clinically indicated, according to Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases.

“With the resources we have, we can’t do everything,” he said, so the question is how to use the findings to have the most impact.

Sustained suppression of HIV in genital secretions is the “most likely” explanation for the reduction in transmission observed in the HIV Prevention Trials Network (HPTN) 052 study, Cohen and colleagues concluded.

The HPTN 052 trial enrolled 1,763 couples, in nine countries, in which one partner was HIV–positive and the other was not. the HIV-positive partners all had relatively robust immune systems and antiretroviral therapy was not indicated according to guidelines.

The HIV-positive partners were randomly assigned to get triple-drug antiretroviral therapy or to wait until the treatment was indicated, with the hypothesis that members of the early-treatment group would be less likely to transmit the virus to their uninfected partners.

A clinical hypothesis was that those getting early treatment would also have a lower risk of serious HIV symptoms: Pulmonary tuberculosis, severe bacterial infection, a World Health Organization stage 4 event, or death.

The HTPN 052 trial was designed with enough statistical power to show a 20% reduction in the risk of transmission, but it was stopped early when an interim analysis showed the risk reduction was 96%, Cohen and colleagues reported.

Indeed, of the 28 transmissions that were genetically linked to the infected partner, only one took place in the early-treatment group (HR 0.04, 9% CI 0.01 to 0.27, P<0.001), they found.

There were 39 cases of HIV transmission, including 11 that could not be linked to the infected partner, the researchers reported. of those, only four were in the early treatment group. the hazard ratio was 0.11 with a 95% confidence interval from 0.04 to 0.32, which was again significant at P<0.001.

Cohen told reporters that the single case of transmission was at best equivocal: the initially uninfected partner was shown to have acquired HIV 85 days after her partner began therapy, but genetic analysis suggested she had been infected more than 50 days and as much as 84 days earlier.

“Our interpretation is that it’s very likely that transmission took place before her partner had enough antiviral to suppress viremia,” Cohen said.

There was also a benefit of early treatment in terms of the primary clinical endpoints, Cohen and colleagues reported. There were 40 such events in the early-therapy group and 65 in the delayed-therapy group (HR 0.59, 95% CI 0.40 to 0.88, P=0.01).

The difference was mainly driven by the incidence of extrapulmonary tuberculosis, seen in three participants in the early-therapy group and 17 in the delayed-therapy group, a difference that was significant at P=0.002.

There was no significant difference between the groups in incidence of pulmonary tuberculosis, they found.

The researchers also reported:

• 82% of the 28 linked transmissions took place in Africa.
• In 18 of the 27 cases in the delayed-treatment group, the source of HIV was a woman; the source of the sole transmission in the early-treatment group was a man.
• 55% of the cases of extrapulmonary tuberculosis were seen in India.
• 97% of the couples were heterosexual and 94% were married.
• 50% of HIV-positive participants were men.
• There were 23 deaths, including 10 in the early-therapy group and 13 in the delayed-therapy group, a difference that was not significant.

Aside from the primary clinical endpoints, 246 HIV-positive participants had one or more severe or life-threatening adverse events, but there was no significant difference between the groups.

The report comes as a series of recent results, including the HPTN 052 trial, has provided “strong encouragement” for the use of antiretroviral drugs to prevent HIV infection, according to Scott Hammer, MD, of Columbia University in new York City.

They include the use of a microbicide gel, containing an anti-HIV drug, to reduce the risk of women acquiring the virus, and a study of oral prophylaxis to prevent infection among men who have sex with men, Hammer noted.

HPTN 052 suggests that there is a “dovetailing of individual and public health benefits” that supports such approaches, Hammer argued in an accompanying editorial in the journal.

But drug therapy as prevention “is not the ultimate answer to controlling and ending the HIV epidemic,” he argued, because of such concerns as adverse events, the possible emergence of drug-resistance, and cost.

Nonetheless, Hammer concluded, such an approach has the “potential to preserve health and control the epidemic until a safe and effective HIV vaccine is a reality.”

The study was supported by the HIV Prevention Trials Network and the National Institute of Allergy and Infectious Diseases. Study drugs were donated by Abbott Laboratories, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, and Merck.

The journal said Cohen did not report any disclosures.

The journal said Hammer reported financial links with Merck and Progenics.

Washington, Mar 8 : Researchers at the Washington University School of Medicine have managed to block the development of multiple sclerosis-like symptoms using a mouse model of the disease.

When scientists gave mice a drug that suppressed the activity of a key molecule, immune cells lined up at the boundaries of the spine instead of going in. Scientists have blocked harmful immune cells from entering the brain in mice with a condition similar to multiple sclerosis (MS).

It is important because MS is apparently caused by misdirected immune cells that enter the brain and damage myelin-an insulating material on the branches of neurons that conduct nerve impulses, said researchers.

“the results were so dramatic that we ended up producing early evidence that this compound might be helpful as a drug for MS. the harmful immune cells were unable to gain access to the brain tissue, and the mice that received the highest dosage were protected from disease,” said Robyn Klein.

Klein and her colleagues discovered a chemical stairway that immune cells have to climb down to enter the brain. Immune cells that exit the blood remain along the vessels on the tissue side, climbing down from the meninges into the brain where they can then cross additional barriers and attack myelin on the branches of neurons.

“the effect of immune cell entry into the brain depends on context. in the case of viral infection, immune cell entry is required to clear the virus. but in autoimmune diseases like multiple sclerosis, their entry is associated with damage so we need to find ways to keep them out,” said Klein.

The stairway is located on the tissue side of the microvasculature, tiny vessels that carry blood into the central nervous system. the steps are made of a molecule called CXCL12 that localizes immune cells, acting like stairs that slow them down so that they can be evaluated to determine if they are allowed to enter the brain.

Klein’s lab previously discovered that the blood vessel cells of the microvasculature display copies of this molecule on their surfaces.

Klein also found that MS causes CXCL12 to be pulled inside blood vessel cells in humans and mice, removing the stairway’s steps and the checkpoints they provide.

In the new paper, she showed that blocking the internalization of the molecule prevented immune cells from getting into the brain and doing harm.

Work by another lab called Klein’s attention to CXCR7, a receptor that binds to CXCL12. she showed that the receptor is made by the same cells in the microvasculature that display CXCL12. they watched the receptor take copies of CXCL12 and dump them in the cells’ lysosomes, pockets for breakdown and recycling of molecules the cell no longer needs.

Klein contacted researchers at ChemoCentryx, who were developing a blocker of the CXCR7 receptor as a cancer treatment. When they gave it to the mouse model of MS, immune cells stopped at the meninges.

The findings have been published in the Journal of Experimental Medicine. (ANI)

I developed flu like symptoms on Wednesday evening and didn't get any sleep that night with aching muscles, high temperature, sore throat and headache. So I phoned in sick yesterday (Thursday). I seem to have made a speedy recovery, just left with the sore throat.
I'm wondering whether I should go in to work today? Physically I could cope with it but would I still be infectious and potentially pass it on to colleagues? I also work with the public including the elderly.

I would say you were definitely still infectious, and in your line of work you definitely can't afford to pass the virus on. I would consult a doctor (even if it is just a telephone consultation) to ask them what they think.

Hi
best stay away till monday, then you will be sure not to have it.
if it was flu and your body dealt with it then fine but you could be infectious.

LONDON – British scientists have developed a preliminary blood test that could one day be used to detect the proteins that cause the human form of mad cow disease, according to a new study.

The disease-carrying proteins, or prions, that cause variant Creutzfeldt-Jakob disease can remain dormant for decades and there are currently no reliable tests to detect them. after the mad cow scare that hit Britain in the 1980s, some experts fear there might be thousands of hidden cases in the country. the department of health estimates one in 4,000 Britons could be infected.

In a study published Thursday in the medical journal Lancet, scientists describe a new blood test that can identify tiny amounts of the prions that cause mad cow disease. John Collinge of the U.K. Medical Research Council Prion Unit and colleagues used their test on 190 blood samples, including 21 people with symptoms of the brain-wasting disease.

The new test correctly identified mad cow disease in 15 patients and was better at picking up small concentrations of the disease-causing proteins than the currently available test. the scientists thought their test might have missed the other six patients because the patients’ levels of prion-causing disease were too low.

“Our findings demonstrate the ability to detect prion infection in blood and show that a donor screening test is technically feasible,” Collinge and colleagues wrote. Mad cow disease can be spread by blood transfusions, surgery or dental procedures. Some experts have called for better ways to protect the population from the degenerative disease.

Variant Creutzfeldt-Jakob disease is usually seen in people who have eaten food products from infected cattle. Patients develop psychiatric symptoms including depression, schizophrenia or psychosis. Most are immobile or mute by the time the disease kills them.

In an accompanying commentary, Luisa Gregori of the U.S. Food and Drug Administration wrote that Collinge and colleagues’ test “represents an important step” towards a diagnostic test for human mad cow disease.

But she warned that for a test to effectively screen large numbers of blood donors, it would need to be much more accurate and capable of detecting the disease in people carrying the disease who did not already have symptoms.

CHICAGO (Reuters) – A pregnancy hormone that relaxes blood vessels appeared to reduce symptoms of acute heart failure and improve survival, according to a preliminary study released by U.S. researchers on Sunday.

They said the hormone relaxin, which is being developed by privately held Corthera Inc of California, was safe, and showed signs of reducing the risk of death from heart problems during the study.

The findings suggest that "early administration of this drug, in addition to standard therapy, might be associated with more rapid, sustained and complete resolution of acute heart failure, as well as with more favorable long-term outcomes," John Teerlink of the University of California, San Francisco, and colleagues wrote in the journal Lancet.

"if established in larger studies, the benefits of relaxin might represent an important advance in the treatment of patients with acute heart failure," the researchers wrote.

In pregnancy, the hormone helps relax and lengthen the cervix to prepare for childbirth, but it is also thought to be a natural vasodilator, widening blood vessels and allowing blood to flow more freely.

Vasodilators are often given to people with high blood pressure, which is common in heart failure, a condition in which the heart gradually loses its ability to pump blood efficiently, leaving organs starved for oxygen.

Teerlink and colleagues studied 234 elderly patients with heart failure and high blood pressure who were given either a 48-hour intravenous infusion of the drug or a placebo.

They found it was safe and helped to reduce shortness of breath in 40 percent of patients who received a moderate dose of the drug, compared with 23 percent who took a placebo.

It also reduced the number of patients in the study who died from heart problems or were readmitted to the hospital within two months for kidney failure compared with the placebo, according to the results, which were also presented at the American College of Cardiology meeting in Florida.

An estimated 5.3 million Americans have heart failure, a chronic but often deadly condition that will cost $34.8 billion this year for direct and indirect U.S. treatment costs, according to the American Heart Association.

© Copyright (c) Reuters

WASHINGTON, D.C.—Parasites get a bad rap for a good reason. they cause a litany of diseases with a terrifying host of symptoms. but mounting evidence suggests that they can also prevent disease. And now there’s genetic evidence to suggest that’s true. new research presented here yesterday at the annual meeting of the American Association for the Advancement of Science (which publishes ScienceNOW) finds that a gene associated with increased risk of asthma is also linked to resistance against a parasitic worm.

Scientists have long suspected that allergies and asthma—common in the developed world and relatively rare in poor countries—are the result of lack of exposure to microbes. this 2-decade-old idea, called the hygiene hypothesis, suggests that lack of exposure to dangerous parasites in childhood makes the adaptive arm of the immune system more likely to overreact when it comes into contact with benign allergens.

Kathleen Barnes, an anthropologist and genetics expert at Johns Hopkins University in Baltimore, Maryland, and her colleagues have been studying the relationship between asthma and one particular parasitic worm, Schistosoma mansoni, in Conde, a cluster of rural fishing villages on the coast of Brazil. the worm is common in the region, and up to 85% of residents are exposed to it.

Previous studies have shown that, in areas like Conde, where parasitic worms are endemic, individuals who produce the most worm-specific antibodies—in particular, an antibody called IgE, which triggers inflammation—tend to be the most resistant to worm infection. According to Barnes’s research, that resistance appears to be about 30% heritable.

The researchers noted that after they administered medication to rid Conde’s residents of worms, the incidence of asthma and allergy symptoms increased. So Barnes hypothesized that the mutations that help individuals fend off parasitic worms might be the same mutations that make them susceptible to asthma and allergies. if an individual produces a lot of IgE in response to a worm, he or she might also produce a lot of IgE in response to an allergen.

The team collected blood and stool samples from 850 people in Conde. they tested their blood for antibodies to the worm to gauge their immune response and searched their stool for worm eggs to determine how heavily they were infected. the researchers decided to focus on genes that have been linked to asthma risk. they were particularly interested in IL-33, a gene linked to inflammation that is overexpressed in the lung tissue of asthmatics compared with people without the disease. “IL-33 stands as one of the strongest candidate genes for asthma to date,” Barnes says.

Barnes and colleagues selected 23 genetic markers throughout the gene and tested whether any of them were associated with worm resistance in the residents of Conde. five of them did show a strong association, and those happened to be the exact same markers that are associated with asthma. “And what we’re most excited about is that the relationship is inverse,” Barnes says. “So a [gene variant] that conferred risk to asthma confers protection against [worm infection].”

The researchers posit that natural selection might favor mutations that protect against worm infection and that those same mutations might inadvertently increase the risk of other diseases, such as asthma. the researchers haven’t yet found the exact mutation responsible for the worm resistance and asthma susceptibility. to find that, they’ll have to “drill down deeper,” Barnes says. She speculates that the culprit may be a mutation located in a genome region that regulates activity of the IL-33 gene.

Jennifer Ingram, a cell biologist who studies asthma at Duke University in Durham, North Carolina, says the finding that deworming medication increased the incidence of asthma symptoms is “striking.” She adds that Barnes’s work is important because it points the field toward molecular mechanisms that might contribute to asthma.

David Van Sickle, a medical anthropologist at the University of Wisconsin, Madison, who presented during the same session as Barnes, points out that the global prevalence estimates for asthma are based largely on asking people whether a physician has ever told them they have asthma. but diagnoses vary from culture to culture. Van Sickle found, for example, that physicians in India are much less likely than doctors in Wisconsin to diagnose a person who has clear symptoms of asthma with the disease. So the true prevalence of asthma in India or other countries could be higher or lower than current estimates. Changes in the prevalence of asthma wouldn’t necessarily nullify the hygiene hypothesis, he says, but they could complicate the picture. still, he says Barnes’s work is “elegant.”

Follow our full coverage of AAAS 2011

SAN ANTONIO—Oxytocin, a hormone with a rosy reputation for getting people to love, trust and generally make nice with one another, can get down and dirty, according to evidence presented on January 28 at the annual meeting of the Society for Personality and Social Psychology.

This brain-altering substance apparently amplifies whatever social proclivities a person already possesses, whether positive or negative, says psychologist Jennifer Bartz of Mount Sinai School of Medicine in new York City.

Previous work has shown that a nasal blast of the hormone encourages a usually trusting person to become more trusting (SN Online: 5/21/08), but now Bartz and her colleagues find that it also makes a highly suspicious person more uncooperative and hostile than ever.

“Oxytocin does not simply make everyone feel more secure, trusting and prosocial,” Bartz says.

These new results raise concerns about plans by some researchers to administer oxytocin to people with autism and other psychiatric conditions that include social difficulties, she adds.

Her team studied 14 people diagnosed with borderline personality disorder and 13 volunteers with no psychiatric conditions. Symptoms of borderline personality disorder include severe insecurity about relationships, fears of abandonment and constant, needy reassurance-seeking from partners.

Borderline personality disorder usually occurs in women, but Bartz’s sample included four men. her group of healthy participants included seven men.

Members of each group played a computer game with an experimenter posing as a research volunteer. in each of three rounds, volunteers had to predict whether their partner would cooperate with them so that each player could make $6 or if the partner would leave the game in order to claim $4 alone.

Volunteers who suspected the partner of bad intent could leave the game early and claim $4 for themselves.

Borderline personality players of both sexes left the game early far more often after receiving an oxytocin nasal spray than after whiffing a placebo spray. Inhaling the hormone prodded their already high levels of hostile suspicion and depleted minimal reserves of trust, Bartz suggests.

Psychiatrically healthy players became more cooperative in the money game after getting oxytocin, relative to their placebo responses.

Nasally inhaling oxytocin also magnifies men’s memories of their mothers as being either supportive or not, Bartz says. her team had 31 men fill out surveys on the quality of their relationships with their mothers up to age 16.

Those who described good maternal relationships remembered mom as substantially more caring and supportive after receiving oxytocin, compared with after inhaling a placebo spray. those whose early home life had been troubled remembered mom as much less caring and supportive after oxytocin, versus placebo.

Bartz’s team initially described oxytocin’s two-sided influence on men’s maternal memories in the Dec. 14 Proceedings of the National Academy of Sciences.

These findings underscore that “oxytocin is not a love hormone; its effects vary in different people,” remarks psychologist Greg Norman of Ohio State University in Columbus.

Norman and his colleagues have found that oxytocin stimulates the heart to beat more in sync with the breathing cycle in people with healthy social lives, but not in people who report constant loneliness.

Other researchers have recently reported that oxytocin stimulates greater trust of members of one’s own ethnic group and greater suspicion of other ethnicities.

 Follow U.S. News Science on Twitter.

Alarming new research shows smoking cannabis can trigger psychotic illness such as schizophrenia almost three years earlier.

A new report which analysed 83 studies involving 22,000 people found people vulnerable to mental health problems are likely to suffer symptoms at a much younger age by using the illicit drug.

The findings confirm that cannabis accelerates the onset of full-blown mental illness, which makes it harder to treat successfully.

A man rolls a joint: Experts claim ‘overwhelming evidence’ shows cannabis triggers schizophrenia and other psychotic disorders

Researchers in Australia behind the latest analysis in the Archives of General Psychiatry journal and British experts are calling for renewed public health warnings about the dangers of cannabis.

They claim ‘overwhelming evidence’ shows it triggers schizophrenia and other psychotic disorders, perhaps through an interaction between genetic and environmental disorders or by disrupting brain development.

Dr Matthew Large and colleagues at the Prince of Wales Hospital, New South Wales, looked at 83 studies involving 8,000 people who used cannabis and other substances and 14,000 people who did not.

They found those who used cannabis developed psychosis about 2.7 years younger than those who did not.

Those who used any type of substance developed psychosis about two years younger, whereas the use of alcohol did not affect the age at which psychosis began.

Typical psychotic events among cannabis users are paranoid ideas, hallucinations, hearing voices or bizarre behaviour.

Dr Large said ‘The results of this study provide strong evidence that reducing cannabis use could delay or even prevent some cases of psychosis.

‘Reducing the use of cannabis could be one of the few ways of altering the outcome of the illness because earlier onset of schizophrenia is associated with a worse prognosis and because other factors associated with age at onset, such as family history and sex, cannot be changed.

‘The results of this study confirm the need for a renewed public health warning about the potential for cannabis use to bring on psychotic illness.’

Previous research shows one-quarter of the population has a strong genetic predisposition to develop psychosis and other schizophrenia-like symptoms after smoking cannabis.

The risk increases more than 10-fold in these people.

Experts warn that anyone with pre-existing mental health problems or family history is at increased risk of mental illness if they use cannabis.

Mary Brett, a trustee of CanSS (Cannabis Skunk Support), said the study’s conclusions provided ‘overwhelming evidence’ of the link between cannabis use and psychosis.

She said ‘We know from research done by the Institute of Psychiatry that adolescents who carry a particular copy of a gene are five times more likely to develop psychosis after smoking cannabis – 10 times if they carry two copies.

‘We’ve been trying to campaign for more awareness and a public health campaign is long overdue.

‘People are not listening to the evidence that psychosis happens quicker and younger to cannabis users, and it’s heartbreaking to see the consequences for individuals and families.’

It was reported yesterday that respected GP Dr Hans-Christian Raabe claims he was sacked as a government drugs adviser for holding ‘embarrassing’ views about homosexuality.

Dr Raabe, a ‘traditional Christian’, was appointed to the Advisory Council on the Misuse of Drugs less than a month ago and has not had the chance to attend a meeting.

Home Office officials said he had failed to disclose being a co-author of a study suggesting a link between homosexuality and paedophilia.

The Advisory Council was the centre of controversy in 2009 when its chairman David Nutt was sacked for insisting cannabis was less harmful than alcohol and tobacco.

MONDAY, Jan. 10 (HealthDay News) — People over age 65 are at increased risk for serious side effects while undergoing latent tuberculosis therapy, a new study finds.

Latent tuberculosis occurs when TB bacteria lurk in the body without making the person sick. the host has no symptoms of TB and is not contagious. however, there is still a chance the bacteria could multiply and cause tuberculosis, which can be fatal if it goes untreated.

Latent TB therapy reduces the chances of developing active TB and is used in Canada and the United States as a way to control the disease. the decision to treat a patient with latent TB therapy depends on his or her risk of developing active disease and of experiencing harmful side effects, explained Dr. Dick Menzies, of the Montreal Chest Institute, and colleagues.

In a six-year study of a large population of more than 9,000 latent TB patients who were treated for tuberculosis and a matching control group that was not treated, Menzies and his colleagues found that a higher percentage of patients undergoing latent TB therapy required hospitalization for serious liver problems that those who went untreated. the excess risk was contributed largely by people over 65, he and his colleagues reported, adding that the risk remained significant even after adjusting for co-existing diseases and other factors.

"our data suggest that the risks of therapy for latent tuberculosis infection are considerable among the elderly and should be considered very carefully before therapy is given," he and his colleagues concluded in the study.

The study was published in the Jan. 10 issue of the Canadian Medical Association Journal.

More information

The U.S. Centers for Disease Control and Prevention has more about tuberculosis.